Microarray analysis identifies Autotaxin, a tumour cell motility and angiogenic factor with lysophospholipase D activity, as a specific target of cell transformation by v-Jun

c-Jun Supports Ribosomal RNA Processing and Nucleolar Localization of RNA Helicase DDX21

“…c-Jun Depletion Inhibits rRNA Processing-We recently reported increased expression of 28 S and 18 S rRNA in cells transformed with the viral oncogenic v-Jun protein (17). As the nucleolus is the site where rRNA processing occurs, identification of several nucleolar proteins associated with c-Jun (5, 6) prompted us to test the hypothesis that c-Jun might be involved in the regulation of rRNA processing.…”

Reversion of the Jun-induced oncogenic phenotype by enhanced synthesis of sialosyllactosylceramide (GM3 ganglioside)

“…Jun-dependent oncogenicity is mediated through aberrant transcriptional controls (1). Numerous genes have been identified that are differentially expressed in Jun-transformed avian and mammalian cells (1,33). However, the functions of these over-or underexpressed genes in the transformation process have not been precisely determined.…”

Transcription factors control invasion: AP-1 the first among equals

“…Fos transformants also differentially express genes that directly regulate the cytoskeleton, including the actin binding protein ezrin and members of the tropomyosin family (Joos and Muller, 1995). Putative Jun targets are also implicated in the invasive phenotype, including the matrix metalloproteinases MMP1, MMP3 and MMP9 (Bos et al, 1999), the ECM associated protein osteonectin/SPARC (Briggs et al, 2002) the protein kinase C substrate SSeCKS (Cohen et al, 2001) and the motility and angiogenic factor, autotaxin (Black et al, 2004). Consistent with these observations, v-fos transformed cells are constitutively invasive in a three-dimensional in vitro invasion assay, indicating that AP-1 activity, in the form of v-Fos expression, is sufficient for invasion in this system (Hennigan et al, 1994).…”